[{"date_updated":"2022-06-10T09:55:08Z","ddc":["000"],"department":[{"_id":"KrCh"}],"file_date_updated":"2020-07-14T12:47:33Z","_id":"653","type":"journal_article","article_type":"original","status":"public","publication_identifier":{"issn":["10614036"]},"publication_status":"published","file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"7050","checksum":"e442dc3b7420a36ec805e9bb45cc1a2e","creator":"dernst","file_size":908099,"date_updated":"2020-07-14T12:47:33Z","file_name":"2017_NatureGenetics_Makohon.pdf","date_created":"2019-11-19T08:13:50Z"}],"language":[{"iso":"eng"}],"issue":"3","volume":49,"ec_funded":1,"abstract":[{"text":"The extent of heterogeneity among driver gene mutations present in naturally occurring metastases - that is, treatment-naive metastatic disease - is largely unknown. To address this issue, we carried out 60× whole-genome sequencing of 26 metastases from four patients with pancreatic cancer. We found that identical mutations in known driver genes were present in every metastatic lesion for each patient studied. Passenger gene mutations, which do not have known or predicted functional consequences, accounted for all intratumoral heterogeneity. Even with respect to these passenger mutations, our analysis suggests that the genetic similarity among the founding cells of metastases was higher than that expected for any two cells randomly taken from a normal tissue. The uniformity of known driver gene mutations among metastases in the same patient has critical and encouraging implications for the success of future targeted therapies in advanced-stage disease.","lang":"eng"}],"oa_version":"Submitted Version","pmid":1,"scopus_import":"1","month":"03","intvolume":" 49","citation":{"chicago":"Makohon Moore, Alvin, Ming Zhang, Johannes Reiter, Ivana Božić, Benjamin Allen, Deepanjan Kundu, Krishnendu Chatterjee, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics. Nature Publishing Group, 2017. https://doi.org/10.1038/ng.3764.","ista":"Makohon Moore A, Zhang M, Reiter J, Božić I, Allen B, Kundu D, Chatterjee K, Wong F, Jiao Y, Kohutek Z, Hong J, Attiyeh M, Javier B, Wood L, Hruban R, Nowak M, Papadopoulos N, Kinzler K, Vogelstein B, Iacobuzio Donahue C. 2017. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 49(3), 358–366.","mla":"Makohon Moore, Alvin, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics, vol. 49, no. 3, Nature Publishing Group, 2017, pp. 358–66, doi:10.1038/ng.3764.","apa":"Makohon Moore, A., Zhang, M., Reiter, J., Božić, I., Allen, B., Kundu, D., … Iacobuzio Donahue, C. (2017). Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. Nature Publishing Group. https://doi.org/10.1038/ng.3764","ama":"Makohon Moore A, Zhang M, Reiter J, et al. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 2017;49(3):358-366. doi:10.1038/ng.3764","short":"A. Makohon Moore, M. Zhang, J. Reiter, I. Božić, B. Allen, D. Kundu, K. Chatterjee, F. Wong, Y. Jiao, Z. Kohutek, J. Hong, M. Attiyeh, B. Javier, L. Wood, R. Hruban, M. Nowak, N. Papadopoulos, K. Kinzler, B. Vogelstein, C. Iacobuzio Donahue, Nature Genetics 49 (2017) 358–366.","ieee":"A. Makohon Moore et al., “Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer,” Nature Genetics, vol. 49, no. 3. Nature Publishing Group, pp. 358–366, 2017."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Alvin","last_name":"Makohon Moore","full_name":"Makohon Moore, Alvin"},{"first_name":"Ming","last_name":"Zhang","full_name":"Zhang, Ming"},{"first_name":"Johannes","id":"4A918E98-F248-11E8-B48F-1D18A9856A87","last_name":"Reiter","orcid":"0000-0002-0170-7353","full_name":"Reiter, Johannes"},{"first_name":"Ivana","last_name":"Božić","full_name":"Božić, Ivana"},{"first_name":"Benjamin","last_name":"Allen","full_name":"Allen, Benjamin"},{"last_name":"Kundu","full_name":"Kundu, Deepanjan","id":"1d4c0f4f-e8a3-11ec-a351-e36772758c45","first_name":"Deepanjan"},{"orcid":"0000-0002-4561-241X","full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","first_name":"Krishnendu"},{"first_name":"Fay","full_name":"Wong, Fay","last_name":"Wong"},{"last_name":"Jiao","full_name":"Jiao, Yuchen","first_name":"Yuchen"},{"first_name":"Zachary","full_name":"Kohutek, Zachary","last_name":"Kohutek"},{"first_name":"Jungeui","last_name":"Hong","full_name":"Hong, Jungeui"},{"full_name":"Attiyeh, Marc","last_name":"Attiyeh","first_name":"Marc"},{"first_name":"Breanna","full_name":"Javier, Breanna","last_name":"Javier"},{"last_name":"Wood","full_name":"Wood, Laura","first_name":"Laura"},{"last_name":"Hruban","full_name":"Hruban, Ralph","first_name":"Ralph"},{"first_name":"Martin","full_name":"Nowak, Martin","last_name":"Nowak"},{"first_name":"Nickolas","full_name":"Papadopoulos, Nickolas","last_name":"Papadopoulos"},{"last_name":"Kinzler","full_name":"Kinzler, Kenneth","first_name":"Kenneth"},{"first_name":"Bert","last_name":"Vogelstein","full_name":"Vogelstein, Bert"},{"first_name":"Christine","full_name":"Iacobuzio Donahue, Christine","last_name":"Iacobuzio Donahue"}],"publist_id":"7092","article_processing_charge":"No","external_id":{"pmid":["28092682"]},"title":"Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer","project":[{"call_identifier":"FP7","_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications","grant_number":"279307"},{"name":"Modern Graph Algorithmic Techniques in Formal Verification","grant_number":"P 23499-N23","call_identifier":"FWF","_id":"2584A770-B435-11E9-9278-68D0E5697425"},{"grant_number":"S11407","name":"Game Theory","call_identifier":"FWF","_id":"25863FF4-B435-11E9-9278-68D0E5697425"}],"has_accepted_license":"1","year":"2017","day":"01","publication":"Nature Genetics","page":"358 - 366","doi":"10.1038/ng.3764","date_published":"2017-03-01T00:00:00Z","date_created":"2018-12-11T11:47:43Z","acknowledgement":"We thank the Memorial Sloan Kettering Cancer Center Molecular Cytology core facility for immunohistochemistry staining. This work was supported by Office of Naval Research grant N00014-16-1-2914, the Bill and Melinda Gates Foundation (OPP1148627), and a gift from B. Wu and E. Larson (M.A.N.), National Institutes of Health grants CA179991 (C.A.I.-D. and I.B.), F31 CA180682 (A.P.M.-M.), CA43460 (B.V.), and P50 CA62924, the Monastra Foundation, the Virginia and D.K. Ludwig Fund for Cancer Research, the Lustgarten Foundation for Pancreatic Cancer Research, the Sol Goldman Center for Pancreatic Cancer Research, the Sol Goldman Sequencing Center, ERC Start grant 279307: Graph Games (J.G.R., D.K., and C.K.), Austrian Science Fund (FWF) grant P23499-N23 (J.G.R., D.K., and C.K.), and FWF NFN grant S11407-N23 RiSE/SHiNE (J.G.R., D.K., and C.K.).","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1},{"title":"Practical graphs for optimal side-channel resistant memory-hard functions","department":[{"_id":"KrPi"}],"author":[{"last_name":"Alwen","full_name":"Alwen, Joel F","first_name":"Joel F","id":"2A8DFA8C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jeremiah","full_name":"Blocki, Jeremiah","last_name":"Blocki"},{"last_name":"Harsha","full_name":"Harsha, Ben","first_name":"Ben"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Alwen, Joel F., et al. “Practical Graphs for Optimal Side-Channel Resistant Memory-Hard Functions.” Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, ACM Press, 2017, pp. 1001–17, doi:10.1145/3133956.3134031.","ieee":"J. F. Alwen, J. Blocki, and B. Harsha, “Practical graphs for optimal side-channel resistant memory-hard functions,” in Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, Dallas, TX, USA, 2017, pp. 1001–1017.","short":"J.F. Alwen, J. Blocki, B. Harsha, in:, Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, ACM Press, 2017, pp. 1001–1017.","ama":"Alwen JF, Blocki J, Harsha B. Practical graphs for optimal side-channel resistant memory-hard functions. In: Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security. ACM Press; 2017:1001-1017. doi:10.1145/3133956.3134031","apa":"Alwen, J. F., Blocki, J., & Harsha, B. (2017). Practical graphs for optimal side-channel resistant memory-hard functions. In Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security (pp. 1001–1017). Dallas, TX, USA: ACM Press. https://doi.org/10.1145/3133956.3134031","chicago":"Alwen, Joel F, Jeremiah Blocki, and Ben Harsha. “Practical Graphs for Optimal Side-Channel Resistant Memory-Hard Functions.” In Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, 1001–17. ACM Press, 2017. https://doi.org/10.1145/3133956.3134031.","ista":"Alwen JF, Blocki J, Harsha B. 2017. Practical graphs for optimal side-channel resistant memory-hard functions. Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security. CCS: Conference on Computer and Communications Security, 1001–1017."},"date_updated":"2021-01-12T08:07:53Z","status":"public","project":[{"_id":"258AA5B2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Teaching Old Crypto New Tricks","grant_number":"682815"}],"type":"conference","conference":{"name":"CCS: Conference on Computer and Communications Security","location":"Dallas, TX, USA","end_date":"2017-11-03","start_date":"2017-10-30"},"_id":"6527","doi":"10.1145/3133956.3134031","date_published":"2017-10-30T00:00:00Z","date_created":"2019-06-06T13:21:29Z","ec_funded":1,"page":"1001-1017","day":"30","language":[{"iso":"eng"}],"publication":"Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security","publication_identifier":{"isbn":["9781450349468"]},"publication_status":"published","year":"2017","month":"10","publisher":"ACM Press","quality_controlled":"1","scopus_import":1,"main_file_link":[{"url":"https://eprint.iacr.org/2017/443","open_access":"1"}],"oa":1,"oa_version":"Submitted Version","abstract":[{"text":"A memory-hard function (MHF) ƒn with parameter n can be computed in sequential time and space n. Simultaneously, a high amortized parallel area-time complexity (aAT) is incurred per evaluation. In practice, MHFs are used to limit the rate at which an adversary (using a custom computational device) can evaluate a security sensitive function that still occasionally needs to be evaluated by honest users (using an off-the-shelf general purpose device). The most prevalent examples of such sensitive functions are Key Derivation Functions (KDFs) and password hashing algorithms where rate limits help mitigate off-line dictionary attacks. As the honest users' inputs to these functions are often (low-entropy) passwords special attention is given to a class of side-channel resistant MHFs called iMHFs.\r\n\r\nEssentially all iMHFs can be viewed as some mode of operation (making n calls to some round function) given by a directed acyclic graph (DAG) with very low indegree. Recently, a combinatorial property of a DAG has been identified (called \"depth-robustness\") which results in good provable security for an iMHF based on that DAG. Depth-robust DAGs have also proven useful in other cryptographic applications. Unfortunately, up till now, all known very depth-robust DAGs are impractically complicated and little is known about their exact (i.e. non-asymptotic) depth-robustness both in theory and in practice.\r\n\r\nIn this work we build and analyze (both formally and empirically) several exceedingly simple and efficient to navigate practical DAGs for use in iMHFs and other applications. For each DAG we:\r\n*Prove that their depth-robustness is asymptotically maximal.\r\n*Prove bounds of at least 3 orders of magnitude better on their exact depth-robustness compared to known bounds for other practical iMHF.\r\n*Implement and empirically evaluate their depth-robustness and aAT against a variety of state-of-the art (and several new) depth-reduction and low aAT attacks. \r\nWe find that, against all attacks, the new DAGs perform significantly better in practice than Argon2i, the most widely deployed iMHF in practice.\r\n\r\nAlong the way we also improve the best known empirical attacks on the aAT of Argon2i by implementing and testing several heuristic versions of a (hitherto purely theoretical) depth-reduction attack. Finally, we demonstrate practicality of our constructions by modifying the Argon2i code base to use one of the new high aAT DAGs. Experimental benchmarks on a standard off-the-shelf CPU show that the new modifications do not adversely affect the impressive throughput of Argon2i (despite seemingly enjoying significantly higher aAT).\r\n","lang":"eng"}]},{"publication_identifier":{"issn":["09501991"]},"publication_status":"published","file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"5139","checksum":"eef22a0f42a55b232cb2d1188a2322cb","file_size":228206,"date_updated":"2020-07-14T12:47:33Z","creator":"system","file_name":"IST-2018-987-v1+1_2017_KichevaRivron__Creating_to.pdf","date_created":"2018-12-12T10:15:20Z"}],"language":[{"iso":"eng"}],"issue":"5","volume":144,"ec_funded":1,"abstract":[{"text":"In November 2016, developmental biologists, synthetic biologists and engineers gathered in Paris for a meeting called ‘Engineering the embryo’. The participants shared an interest in exploring how synthetic systems can reveal new principles of embryonic development, and how the in vitro manipulation and modeling of development using stem cells can be used to integrate ideas and expertise from physics, developmental biology and tissue engineering. As we review here, the conference pinpointed some of the challenges arising at the intersection of these fields, along with great enthusiasm for finding new approaches and collaborations.","lang":"eng"}],"oa_version":"Submitted Version","scopus_import":1,"month":"03","intvolume":" 144","date_updated":"2021-01-12T08:07:54Z","ddc":["571"],"department":[{"_id":"AnKi"}],"file_date_updated":"2020-07-14T12:47:33Z","_id":"654","type":"journal_article","status":"public","pubrep_id":"987","has_accepted_license":"1","year":"2017","day":"01","publication":"Development","page":"733 - 736","date_published":"2017-03-01T00:00:00Z","doi":"10.1242/dev.144915","date_created":"2018-12-11T11:47:44Z","publisher":"Company of Biologists","quality_controlled":"1","oa":1,"citation":{"mla":"Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” Development, vol. 144, no. 5, Company of Biologists, 2017, pp. 733–36, doi:10.1242/dev.144915.","apa":"Kicheva, A., & Rivron, N. (2017). Creating to understand – developmental biology meets engineering in Paris. Development. Company of Biologists. https://doi.org/10.1242/dev.144915","ama":"Kicheva A, Rivron N. Creating to understand – developmental biology meets engineering in Paris. Development. 2017;144(5):733-736. doi:10.1242/dev.144915","ieee":"A. Kicheva and N. Rivron, “Creating to understand – developmental biology meets engineering in Paris,” Development, vol. 144, no. 5. Company of Biologists, pp. 733–736, 2017.","short":"A. Kicheva, N. Rivron, Development 144 (2017) 733–736.","chicago":"Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.144915.","ista":"Kicheva A, Rivron N. 2017. Creating to understand – developmental biology meets engineering in Paris. Development. 144(5), 733–736."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"7089","author":[{"id":"3959A2A0-F248-11E8-B48F-1D18A9856A87","first_name":"Anna","last_name":"Kicheva","full_name":"Kicheva, Anna","orcid":"0000-0003-4509-4998"},{"first_name":"Nicolas","last_name":"Rivron","full_name":"Rivron, Nicolas"}],"title":"Creating to understand – developmental biology meets engineering in Paris","project":[{"_id":"B6FC0238-B512-11E9-945C-1524E6697425","call_identifier":"H2020","grant_number":"680037","name":"Coordination of Patterning And Growth In the Spinal Cord"}]},{"abstract":[{"lang":"eng","text":"This paper studies the complexity of estimating Rényi divergences of discrete distributions: p observed from samples and the baseline distribution q known a priori. Extending the results of Acharya et al. (SODA'15) on estimating Rényi entropy, we present improved estimation techniques together with upper and lower bounds on the sample complexity. We show that, contrarily to estimating Rényi entropy where a sublinear (in the alphabet size) number of samples suffices, the sample complexity is heavily dependent on events occurring unlikely in q, and is unbounded in general (no matter what an estimation technique is used). For any divergence of integer order bigger than 1, we provide upper and lower bounds on the number of samples dependent on probabilities of p and q (the lower bounds hold for non-integer orders as well). We conclude that the worst-case sample complexity is polynomial in the alphabet size if and only if the probabilities of q are non-negligible. This gives theoretical insights into heuristics used in the applied literature to handle numerical instability, which occurs for small probabilities of q. Our result shows that they should be handled with care not only because of numerical issues, but also because of a blow up in the sample complexity."}],"oa_version":"Preprint","main_file_link":[{"url":"https://arxiv.org/abs/1702.01666","open_access":"1"}],"scopus_import":1,"month":"08","publication_status":"published","publication_identifier":{"isbn":["9781509040964"]},"language":[{"iso":"eng"}],"ec_funded":1,"_id":"6526","conference":{"name":"ISIT: International Symposium on Information Theory","start_date":"2017-06-25","location":"Aachen, Germany","end_date":"2017-06-30"},"type":"conference","status":"public","date_updated":"2021-01-12T08:07:53Z","department":[{"_id":"KrPi"}],"oa":1,"quality_controlled":"1","publisher":"IEEE","year":"2017","publication":"2017 IEEE International Symposium on Information Theory (ISIT)","day":"09","date_created":"2019-06-06T12:53:09Z","date_published":"2017-08-09T00:00:00Z","doi":"10.1109/isit.2017.8006529","article_number":"8006529","project":[{"_id":"258AA5B2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Teaching Old Crypto New Tricks","grant_number":"682815"}],"citation":{"mla":"Skórski, Maciej. “On the Complexity of Estimating Rènyi Divergences.” 2017 IEEE International Symposium on Information Theory (ISIT), 8006529, IEEE, 2017, doi:10.1109/isit.2017.8006529.","short":"M. Skórski, in:, 2017 IEEE International Symposium on Information Theory (ISIT), IEEE, 2017.","ieee":"M. Skórski, “On the complexity of estimating Rènyi divergences,” in 2017 IEEE International Symposium on Information Theory (ISIT), Aachen, Germany, 2017.","apa":"Skórski, M. (2017). On the complexity of estimating Rènyi divergences. In 2017 IEEE International Symposium on Information Theory (ISIT). Aachen, Germany: IEEE. https://doi.org/10.1109/isit.2017.8006529","ama":"Skórski M. On the complexity of estimating Rènyi divergences. In: 2017 IEEE International Symposium on Information Theory (ISIT). IEEE; 2017. doi:10.1109/isit.2017.8006529","chicago":"Skórski, Maciej. “On the Complexity of Estimating Rènyi Divergences.” In 2017 IEEE International Symposium on Information Theory (ISIT). IEEE, 2017. https://doi.org/10.1109/isit.2017.8006529.","ista":"Skórski M. 2017. On the complexity of estimating Rènyi divergences. 2017 IEEE International Symposium on Information Theory (ISIT). ISIT: International Symposium on Information Theory, 8006529."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","external_id":{"arxiv":["1702.01666"]},"author":[{"id":"EC09FA6A-02D0-11E9-8223-86B7C91467DD","first_name":"Maciej","last_name":"Skórski","full_name":"Skórski, Maciej"}],"title":"On the complexity of estimating Rènyi divergences"},{"status":"public","pubrep_id":"904","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"655","file_date_updated":"2020-07-14T12:47:33Z","department":[{"_id":"CaGu"}],"ddc":["579"],"date_updated":"2021-01-12T08:07:55Z","month":"03","intvolume":" 6","scopus_import":1,"oa_version":"Published Version","abstract":[{"text":"The bacterial flagellum is a self-assembling nanomachine. The external flagellar filament, several times longer than a bacterial cell body, is made of a few tens of thousands subunits of a single protein: flagellin. A fundamental problem concerns the molecular mechanism of how the flagellum grows outside the cell, where no discernible energy source is available. Here, we monitored the dynamic assembly of individual flagella using in situ labelling and real-time immunostaining of elongating flagellar filaments. We report that the rate of flagellum growth, initially ~1,700 amino acids per second, decreases with length and that the previously proposed chain mechanism does not contribute to the filament elongation dynamics. Inhibition of the proton motive force-dependent export apparatus revealed a major contribution of substrate injection in driving filament elongation. The combination of experimental and mathematical evidence demonstrates that a simple, injection-diffusion mechanism controls bacterial flagella growth outside the cell.","lang":"eng"}],"volume":6,"file":[{"checksum":"39e1c3e82ddac83a30422fa72fa1a383","file_id":"4716","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"IST-2017-904-v1+1_elife-23136-v2.pdf","date_created":"2018-12-12T10:08:53Z","file_size":5520359,"date_updated":"2020-07-14T12:47:33Z","creator":"system"},{"creator":"system","file_size":11242920,"date_updated":"2020-07-14T12:47:33Z","file_name":"IST-2017-904-v1+2_elife-23136-figures-v2.pdf","date_created":"2018-12-12T10:08:54Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"4717","checksum":"a6d542253028f52e00aa29739ddffe8f"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050084X"]},"publication_status":"published","article_number":"e23136","title":"Bacterial flagella grow through an injection diffusion mechanism","author":[{"first_name":"Thibaud","last_name":"Renault","full_name":"Renault, Thibaud"},{"first_name":"Anthony","last_name":"Abraham","full_name":"Abraham, Anthony"},{"full_name":"Bergmiller, Tobias","orcid":"0000-0001-5396-4346","last_name":"Bergmiller","first_name":"Tobias","id":"2C471CFA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Guillaume","full_name":"Paradis, Guillaume","last_name":"Paradis"},{"last_name":"Rainville","full_name":"Rainville, Simon","first_name":"Simon"},{"first_name":"Emmanuelle","last_name":"Charpentier","full_name":"Charpentier, Emmanuelle"},{"id":"47F8433E-F248-11E8-B48F-1D18A9856A87","first_name":"Calin C","orcid":"0000-0001-6220-2052","full_name":"Guet, Calin C","last_name":"Guet"},{"last_name":"Tu","full_name":"Tu, Yuhai","first_name":"Yuhai"},{"full_name":"Namba, Keiichi","last_name":"Namba","first_name":"Keiichi"},{"first_name":"James","last_name":"Keener","full_name":"Keener, James"},{"last_name":"Minamino","full_name":"Minamino, Tohru","first_name":"Tohru"},{"full_name":"Erhardt, Marc","last_name":"Erhardt","first_name":"Marc"}],"publist_id":"7082","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis, Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.23136.","ista":"Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E, Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella grow through an injection diffusion mechanism. eLife. 6, e23136.","mla":"Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136.","short":"T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier, C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017).","ieee":"T. Renault et al., “Bacterial flagella grow through an injection diffusion mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017.","ama":"Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136","apa":"Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier, E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136"},"quality_controlled":"1","publisher":"eLife Sciences Publications","oa":1,"doi":"10.7554/eLife.23136","date_published":"2017-03-06T00:00:00Z","date_created":"2018-12-11T11:47:44Z","day":"06","publication":"eLife","has_accepted_license":"1","year":"2017"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Möller B, Ten Hove C, Xiang D, Williams N, López L, Yoshida S, Smit M, Datla R, Weijers D. 2017. Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. 114(12), E2533–E2539.","chicago":"Möller, Barbara, Colette Ten Hove, Daoquan Xiang, Nerys Williams, Lorena López, Saiko Yoshida, Margot Smit, Raju Datla, and Dolf Weijers. “Auxin Response Cell Autonomously Controls Ground Tissue Initiation in the Early Arabidopsis Embryo.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1616493114.","ama":"Möller B, Ten Hove C, Xiang D, et al. Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. 2017;114(12):E2533-E2539. doi:10.1073/pnas.1616493114","apa":"Möller, B., Ten Hove, C., Xiang, D., Williams, N., López, L., Yoshida, S., … Weijers, D. (2017). Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1616493114","short":"B. Möller, C. Ten Hove, D. Xiang, N. Williams, L. López, S. Yoshida, M. Smit, R. Datla, D. Weijers, PNAS 114 (2017) E2533–E2539.","ieee":"B. Möller et al., “Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo,” PNAS, vol. 114, no. 12. National Academy of Sciences, pp. E2533–E2539, 2017.","mla":"Möller, Barbara, et al. “Auxin Response Cell Autonomously Controls Ground Tissue Initiation in the Early Arabidopsis Embryo.” PNAS, vol. 114, no. 12, National Academy of Sciences, 2017, pp. E2533–39, doi:10.1073/pnas.1616493114."},"title":"Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo","author":[{"full_name":"Möller, Barbara","last_name":"Möller","first_name":"Barbara"},{"last_name":"Ten Hove","full_name":"Ten Hove, Colette","first_name":"Colette"},{"last_name":"Xiang","full_name":"Xiang, Daoquan","first_name":"Daoquan"},{"first_name":"Nerys","last_name":"Williams","full_name":"Williams, Nerys"},{"first_name":"Lorena","full_name":"López, Lorena","last_name":"López"},{"first_name":"Saiko","id":"2E46069C-F248-11E8-B48F-1D18A9856A87","full_name":"Yoshida, Saiko","last_name":"Yoshida"},{"first_name":"Margot","full_name":"Smit, Margot","last_name":"Smit"},{"first_name":"Raju","full_name":"Datla, Raju","last_name":"Datla"},{"last_name":"Weijers","full_name":"Weijers, Dolf","first_name":"Dolf"}],"publist_id":"7076","external_id":{"pmid":["28265057"]},"publisher":"National Academy of Sciences","quality_controlled":"1","oa":1,"day":"21","publication":"PNAS","year":"2017","doi":"10.1073/pnas.1616493114","date_published":"2017-03-21T00:00:00Z","date_created":"2018-12-11T11:47:45Z","page":"E2533 - E2539","_id":"657","status":"public","type":"journal_article","date_updated":"2021-01-12T08:08:02Z","department":[{"_id":"JiFr"}],"pmid":1,"oa_version":"Submitted Version","abstract":[{"text":"Plant organs are typically organized into three main tissue layers. The middle ground tissue layer comprises the majority of the plant body and serves a wide range of functions, including photosynthesis, selective nutrient uptake and storage, and gravity sensing. Ground tissue patterning and maintenance in Arabidopsis are controlled by a well-established gene network revolving around the key regulator SHORT-ROOT (SHR). In contrast, it is completely unknown how ground tissue identity is first specified from totipotent precursor cells in the embryo. The plant signaling molecule auxin, acting through AUXIN RESPONSE FACTOR (ARF) transcription factors, is critical for embryo patterning. The auxin effector ARF5/MONOPTEROS (MP) acts both cell-autonomously and noncell-autonomously to control embryonic vascular tissue formation and root initiation, respectively. Here we show that auxin response and ARF activity cell-autonomously control the asymmetric division of the first ground tissue cells. By identifying embryonic target genes, we show that MP transcriptionally initiates the ground tissue lineage and acts upstream of the regulatory network that controls ground tissue patterning and maintenance. Strikingly, whereas the SHR network depends on MP, this MP function is, at least in part, SHR independent. Our study therefore identifies auxin response as a regulator of ground tissue specification in the embryonic root, and reveals that ground tissue initiation and maintenance use different regulators and mechanisms. Moreover, our data provide a framework for the simultaneous formation of multiple cell types by the same transcriptional regulator.","lang":"eng"}],"month":"03","intvolume":" 114","scopus_import":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373392/","open_access":"1"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["00278424"]},"publication_status":"published","issue":"12","volume":114},{"oa_version":"None","abstract":[{"text":"Human neurons transplanted into a mouse model for Alzheimer’s disease show human-specific vulnerability to β-amyloid plaques and may help to identify new therapeutic targets.","lang":"eng"}],"month":"03","intvolume":" 9","publisher":"American Association for the Advancement of Science","quality_controlled":"1","scopus_import":1,"day":"15","language":[{"iso":"eng"}],"publication":"Science Translational Medicine","publication_identifier":{"issn":["19466234"]},"year":"2017","publication_status":"published","volume":9,"issue":"381","doi":"10.1126/scitranslmed.aam9867","date_published":"2017-03-15T00:00:00Z","date_created":"2018-12-11T11:47:45Z","article_number":"eaam9867","_id":"656","status":"public","type":"journal_article","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T08:07:59Z","citation":{"ista":"Novarino G. 2017. Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. 9(381), eaam9867.","chicago":"Novarino, Gaia. “Modeling Alzheimer’s Disease in Mice with Human Neurons.” Science Translational Medicine. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/scitranslmed.aam9867.","apa":"Novarino, G. (2017). Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. American Association for the Advancement of Science. https://doi.org/10.1126/scitranslmed.aam9867","ama":"Novarino G. Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. 2017;9(381). doi:10.1126/scitranslmed.aam9867","ieee":"G. Novarino, “Modeling Alzheimer’s disease in mice with human neurons,” Science Translational Medicine, vol. 9, no. 381. American Association for the Advancement of Science, 2017.","short":"G. Novarino, Science Translational Medicine 9 (2017).","mla":"Novarino, Gaia. “Modeling Alzheimer’s Disease in Mice with Human Neurons.” Science Translational Medicine, vol. 9, no. 381, eaam9867, American Association for the Advancement of Science, 2017, doi:10.1126/scitranslmed.aam9867."},"department":[{"_id":"GaNo"}],"title":"Modeling Alzheimer's disease in mice with human neurons","publist_id":"7079","author":[{"id":"3E57A680-F248-11E8-B48F-1D18A9856A87","first_name":"Gaia","last_name":"Novarino","orcid":"0000-0002-7673-7178","full_name":"Novarino, Gaia"}]},{"publication_status":"published","publication_identifier":{"issn":["16625218"]},"language":[{"iso":"eng"}],"file":[{"file_name":"IST-2017-903-v1+1_fnbot-11-00008.pdf","date_created":"2018-12-12T10:18:49Z","creator":"system","file_size":8439566,"date_updated":"2020-07-14T12:47:33Z","file_id":"5371","checksum":"b1bc43f96d1df3313c03032c2a46388d","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"ec_funded":1,"issue":"MAR","volume":11,"abstract":[{"text":"With the accelerated development of robot technologies, control becomes one of the central themes of research. In traditional approaches, the controller, by its internal functionality, finds appropriate actions on the basis of specific objectives for the task at hand. While very successful in many applications, self-organized control schemes seem to be favored in large complex systems with unknown dynamics or which are difficult to model. Reasons are the expected scalability, robustness, and resilience of self-organizing systems. The paper presents a self-learning neurocontroller based on extrinsic differential plasticity introduced recently, applying it to an anthropomorphic musculoskeletal robot arm with attached objects of unknown physical dynamics. The central finding of the paper is the following effect: by the mere feedback through the internal dynamics of the object, the robot is learning to relate each of the objects with a very specific sensorimotor pattern. Specifically, an attached pendulum pilots the arm into a circular motion, a half-filled bottle produces axis oriented shaking behavior, a wheel is getting rotated, and wiping patterns emerge automatically in a table-plus-brush setting. By these object-specific dynamical patterns, the robot may be said to recognize the object's identity, or in other words, it discovers dynamical affordances of objects. Furthermore, when including hand coordinates obtained from a camera, a dedicated hand-eye coordination self-organizes spontaneously. These phenomena are discussed from a specific dynamical system perspective. Central is the dedicated working regime at the border to instability with its potentially infinite reservoir of (limit cycle) attractors "waiting" to be excited. Besides converging toward one of these attractors, variate behavior is also arising from a self-induced attractor morphing driven by the learning rule. We claim that experimental investigations with this anthropomorphic, self-learning robot not only generate interesting and potentially useful behaviors, but may also help to better understand what subjective human muscle feelings are, how they can be rooted in sensorimotor patterns, and how these concepts may feed back on robotics.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 11","month":"03","date_updated":"2021-01-12T08:08:04Z","ddc":["006"],"file_date_updated":"2020-07-14T12:47:33Z","department":[{"_id":"ChLa"},{"_id":"GaTk"}],"_id":"658","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"903","status":"public","year":"2017","has_accepted_license":"1","publication":"Frontiers in Neurorobotics","day":"16","date_created":"2018-12-11T11:47:45Z","date_published":"2017-03-16T00:00:00Z","doi":"10.3389/fnbot.2017.00008","oa":1,"quality_controlled":"1","publisher":"Frontiers Research Foundation","citation":{"apa":"Der, R., & Martius, G. S. (2017). Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. Frontiers Research Foundation. https://doi.org/10.3389/fnbot.2017.00008","ama":"Der R, Martius GS. Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. 2017;11(MAR). doi:10.3389/fnbot.2017.00008","ieee":"R. Der and G. S. Martius, “Self organized behavior generation for musculoskeletal robots,” Frontiers in Neurorobotics, vol. 11, no. MAR. Frontiers Research Foundation, 2017.","short":"R. Der, G.S. Martius, Frontiers in Neurorobotics 11 (2017).","mla":"Der, Ralf, and Georg S. Martius. “Self Organized Behavior Generation for Musculoskeletal Robots.” Frontiers in Neurorobotics, vol. 11, no. MAR, 00008, Frontiers Research Foundation, 2017, doi:10.3389/fnbot.2017.00008.","ista":"Der R, Martius GS. 2017. Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. 11(MAR), 00008.","chicago":"Der, Ralf, and Georg S Martius. “Self Organized Behavior Generation for Musculoskeletal Robots.” Frontiers in Neurorobotics. Frontiers Research Foundation, 2017. https://doi.org/10.3389/fnbot.2017.00008."},"user_id":"2EBD1598-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes","author":[{"first_name":"Ralf","last_name":"Der","full_name":"Der, Ralf"},{"last_name":"Martius","full_name":"Martius, Georg S","first_name":"Georg S","id":"3A276B68-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"7078","title":"Self organized behavior generation for musculoskeletal robots","article_number":"00008","project":[{"_id":"25681D80-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"291734","name":"International IST Postdoc Fellowship Programme"}]},{"department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:34Z","date_updated":"2021-01-12T08:08:06Z","ddc":["570"],"type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","pubrep_id":"902","_id":"659","volume":8,"publication_identifier":{"issn":["20411723"]},"publication_status":"published","file":[{"content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"5072","checksum":"dae30190291c3630e8102d8714a8d23e","date_updated":"2020-07-14T12:47:34Z","file_size":9523746,"creator":"system","date_created":"2018-12-12T10:14:21Z","file_name":"IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf"}],"language":[{"iso":"eng"}],"scopus_import":1,"month":"03","intvolume":" 8","abstract":[{"text":"Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching.","lang":"eng"}],"oa_version":"Published Version","publist_id":"7075","author":[{"last_name":"Kage","full_name":"Kage, Frieda","first_name":"Frieda"},{"first_name":"Moritz","full_name":"Winterhoff, Moritz","last_name":"Winterhoff"},{"full_name":"Dimchev, Vanessa","last_name":"Dimchev","first_name":"Vanessa"},{"full_name":"Müller, Jan","last_name":"Müller","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan"},{"first_name":"Tobias","full_name":"Thalheim, Tobias","last_name":"Thalheim"},{"first_name":"Anika","full_name":"Freise, Anika","last_name":"Freise"},{"first_name":"Stefan","last_name":"Brühmann","full_name":"Brühmann, Stefan"},{"full_name":"Kollasser, Jana","last_name":"Kollasser","first_name":"Jana"},{"first_name":"Jennifer","last_name":"Block","full_name":"Block, Jennifer"},{"first_name":"Georgi A","full_name":"Dimchev, Georgi A","last_name":"Dimchev"},{"first_name":"Matthias","full_name":"Geyer, Matthias","last_name":"Geyer"},{"last_name":"Schnittler","full_name":"Schnittler, Hams","first_name":"Hams"},{"first_name":"Cord","last_name":"Brakebusch","full_name":"Brakebusch, Cord"},{"full_name":"Stradal, Theresia","last_name":"Stradal","first_name":"Theresia"},{"last_name":"Carlier","full_name":"Carlier, Marie","first_name":"Marie"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"full_name":"Käs, Josef","last_name":"Käs","first_name":"Josef"},{"first_name":"Jan","full_name":"Faix, Jan","last_name":"Faix"},{"last_name":"Rottner","full_name":"Rottner, Klemens","first_name":"Klemens"}],"article_processing_charge":"No","title":"FMNL formins boost lamellipodial force generation","citation":{"ista":"Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832.","chicago":"Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832.","ama":"Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832","apa":"Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832","short":"F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017).","ieee":"F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017.","mla":"Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","article_number":"14832","date_published":"2017-03-22T00:00:00Z","doi":"10.1038/ncomms14832","date_created":"2018-12-11T11:47:46Z","has_accepted_license":"1","year":"2017","day":"22","publication":"Nature Communications","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1},{"_id":"660","type":"journal_article","status":"public","date_updated":"2021-01-12T08:08:09Z","department":[{"_id":"MaLo"}],"abstract":[{"lang":"eng","text":"Growing microtubules are protected from depolymerization by the presence of a GTP or GDP/Pi cap. End-binding proteins of the EB1 family bind to the stabilizing cap, allowing monitoring of its size in real time. The cap size has been shown to correlate with instantaneous microtubule stability. Here we have quantitatively characterized the properties of cap size fluctuations during steadystate growth and have developed a theory predicting their timescale and amplitude from the kinetics of microtubule growth and cap maturation. In contrast to growth speed fluctuations, cap size fluctuations show a characteristic timescale, which is defined by the lifetime of the cap sites. Growth fluctuations affect the amplitude of cap size fluctuations; however, cap size does not affect growth speed, indicating that microtubules are far from instability during most of their time of growth. Our theory provides the basis for a quantitative understanding of microtubule stability fluctuations during steady-state growth."}],"oa_version":"Submitted Version","pmid":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380103/","open_access":"1"}],"scopus_import":1,"intvolume":" 114","month":"03","publication_status":"published","publication_identifier":{"issn":["00278424"]},"language":[{"iso":"eng"}],"volume":114,"issue":"13","citation":{"ista":"Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. 2017. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. 114(13), 3427–3432.","chicago":"Rickman, Jamie, Christian F Düllberg, Nicholas Cade, Lewis Griffin, and Thomas Surrey. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1620274114.","ieee":"J. Rickman, C. F. Düllberg, N. Cade, L. Griffin, and T. Surrey, “Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation,” PNAS, vol. 114, no. 13. National Academy of Sciences, pp. 3427–3432, 2017.","short":"J. Rickman, C.F. Düllberg, N. Cade, L. Griffin, T. Surrey, PNAS 114 (2017) 3427–3432.","ama":"Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. 2017;114(13):3427-3432. doi:10.1073/pnas.1620274114","apa":"Rickman, J., Düllberg, C. F., Cade, N., Griffin, L., & Surrey, T. (2017). Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1620274114","mla":"Rickman, Jamie, et al. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” PNAS, vol. 114, no. 13, National Academy of Sciences, 2017, pp. 3427–32, doi:10.1073/pnas.1620274114."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","external_id":{"pmid":["28280102"]},"author":[{"first_name":"Jamie","last_name":"Rickman","full_name":"Rickman, Jamie"},{"full_name":"Düllberg, Christian F","orcid":"0000-0001-6335-9748","last_name":"Düllberg","id":"459064DC-F248-11E8-B48F-1D18A9856A87","first_name":"Christian F"},{"first_name":"Nicholas","last_name":"Cade","full_name":"Cade, Nicholas"},{"last_name":"Griffin","full_name":"Griffin, Lewis","first_name":"Lewis"},{"first_name":"Thomas","full_name":"Surrey, Thomas","last_name":"Surrey"}],"publist_id":"7073","title":"Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation","acknowledgement":"We thank Philippe Cluzel for helpful discussions and Gunnar Pruessner for data analysis advice. This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK Grant FC001163, Medical Research Council Grant FC001163, and Wellcome Trust Grant FC001163. This work was also supported by European Research Council Advanced Grant Project 323042 (to C.D. and T.S.).","oa":1,"publisher":"National Academy of Sciences","quality_controlled":"1","year":"2017","publication":"PNAS","day":"28","page":"3427 - 3432","date_created":"2018-12-11T11:47:46Z","date_published":"2017-03-28T00:00:00Z","doi":"10.1073/pnas.1620274114"},{"oa":1,"quality_controlled":"1","publisher":"American Institute of Physics","date_created":"2018-12-11T11:47:47Z","doi":"10.1063/1.4981525","date_published":"2017-04-01T00:00:00Z","publication":"Physics of Fluids","day":"01","year":"2017","project":[{"_id":"2511D90C-B435-11E9-9278-68D0E5697425","name":"Astrophysical instability of currents and turbulences","grant_number":"SFB 963 TP A8"}],"article_number":"044107","title":"Hydrodynamic turbulence in quasi Keplerian rotating flows","author":[{"last_name":"Shi","full_name":"Shi, Liang","first_name":"Liang"},{"full_name":"Hof, Björn","orcid":"0000-0003-2057-2754","last_name":"Hof","id":"3A374330-F248-11E8-B48F-1D18A9856A87","first_name":"Björn"},{"first_name":"Markus","last_name":"Rampp","full_name":"Rampp, Markus"},{"full_name":"Avila, Marc","last_name":"Avila","first_name":"Marc"}],"publist_id":"7072","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"apa":"Shi, L., Hof, B., Rampp, M., & Avila, M. (2017). Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. American Institute of Physics. https://doi.org/10.1063/1.4981525","ama":"Shi L, Hof B, Rampp M, Avila M. Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. 2017;29(4). doi:10.1063/1.4981525","ieee":"L. Shi, B. Hof, M. Rampp, and M. Avila, “Hydrodynamic turbulence in quasi Keplerian rotating flows,” Physics of Fluids, vol. 29, no. 4. American Institute of Physics, 2017.","short":"L. Shi, B. Hof, M. Rampp, M. Avila, Physics of Fluids 29 (2017).","mla":"Shi, Liang, et al. “Hydrodynamic Turbulence in Quasi Keplerian Rotating Flows.” Physics of Fluids, vol. 29, no. 4, 044107, American Institute of Physics, 2017, doi:10.1063/1.4981525.","ista":"Shi L, Hof B, Rampp M, Avila M. 2017. Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. 29(4), 044107.","chicago":"Shi, Liang, Björn Hof, Markus Rampp, and Marc Avila. “Hydrodynamic Turbulence in Quasi Keplerian Rotating Flows.” Physics of Fluids. American Institute of Physics, 2017. https://doi.org/10.1063/1.4981525."},"intvolume":" 29","month":"04","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1703.01714"}],"scopus_import":1,"oa_version":"Submitted Version","abstract":[{"lang":"eng","text":"We report a direct-numerical-simulation study of the Taylor-Couette flow in the quasi-Keplerian regime at shear Reynolds numbers up to (105). Quasi-Keplerian rotating flow has been investigated for decades as a simplified model system to study the origin of turbulence in accretion disks that is not fully understood. The flow in this study is axially periodic and thus the experimental end-wall effects on the stability of the flow are avoided. Using optimal linear perturbations as initial conditions, our simulations find no sustained turbulence: the strong initial perturbations distort the velocity profile and trigger turbulence that eventually decays."}],"issue":"4","volume":29,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["10706631"]},"status":"public","type":"journal_article","_id":"662","department":[{"_id":"BjHo"}],"date_updated":"2021-01-12T08:08:15Z"},{"scopus_import":1,"month":"04","abstract":[{"text":"In this paper, we propose an approach to automatically compute invariant clusters for nonlinear semialgebraic hybrid systems. An invariant cluster for an ordinary differential equation (ODE) is a multivariate polynomial invariant g(u→, x→) = 0, parametric in u→, which can yield an infinite number of concrete invariants by assigning different values to u→ so that every trajectory of the system can be overapproximated precisely by the intersection of a group of concrete invariants. For semialgebraic systems, which involve ODEs with multivariate polynomial right-hand sides, given a template multivariate polynomial g(u→, x→), an invariant cluster can be obtained by first computing the remainder of the Lie derivative of g(u→, x→) divided by g(u→, x→) and then solving the system of polynomial equations obtained from the coefficients of the remainder. Based on invariant clusters and sum-of-squares (SOS) programming, we present a new method for the safety verification of hybrid systems. Experiments on nonlinear benchmark systems from biology and control theory show that our approach is efficient. ","lang":"eng"}],"oa_version":"Submitted Version","publication_status":"published","publication_identifier":{"isbn":["978-145034590-3"]},"language":[{"iso":"eng"}],"file":[{"date_created":"2018-12-12T10:11:20Z","file_name":"IST-2017-817-v1+1_p163-kong.pdf","date_updated":"2020-07-14T12:47:34Z","file_size":1650530,"creator":"system","checksum":"b7667434cbf5b5f0ade3bea1dbe5bf63","file_id":"4873","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"conference":{"name":"HSCC: Hybrid Systems Computation and Control ","start_date":"2017-04-18","location":"Pittsburgh, PA, United States","end_date":"2017-04-20"},"type":"conference","pubrep_id":"817","status":"public","_id":"663","file_date_updated":"2020-07-14T12:47:34Z","department":[{"_id":"ToHe"}],"date_updated":"2021-01-12T08:08:17Z","ddc":["000"],"oa":1,"quality_controlled":"1","publisher":"ACM","page":"163 - 172","date_created":"2018-12-11T11:47:47Z","doi":"10.1145/3049797.3049814","date_published":"2017-04-01T00:00:00Z","year":"2017","has_accepted_license":"1","publication":"Proceedings of the 20th International Conference on Hybrid Systems","day":"01","publist_id":"7067","author":[{"orcid":"0000-0002-3066-6941","full_name":"Kong, Hui","last_name":"Kong","id":"3BDE25AA-F248-11E8-B48F-1D18A9856A87","first_name":"Hui"},{"first_name":"Sergiy","full_name":"Bogomolov, Sergiy","orcid":"0000-0002-0686-0365","last_name":"Bogomolov"},{"last_name":"Schilling","full_name":"Schilling, Christian","first_name":"Christian"},{"first_name":"Yu","full_name":"Jiang, Yu","last_name":"Jiang"},{"id":"40876CD8-F248-11E8-B48F-1D18A9856A87","first_name":"Thomas A","last_name":"Henzinger","orcid":"0000−0002−2985−7724","full_name":"Henzinger, Thomas A"}],"title":"Safety verification of nonlinear hybrid systems based on invariant clusters","citation":{"ista":"Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. 2017. Safety verification of nonlinear hybrid systems based on invariant clusters. Proceedings of the 20th International Conference on Hybrid Systems. HSCC: Hybrid Systems Computation and Control , 163–172.","chicago":"Kong, Hui, Sergiy Bogomolov, Christian Schilling, Yu Jiang, and Thomas A Henzinger. “Safety Verification of Nonlinear Hybrid Systems Based on Invariant Clusters.” In Proceedings of the 20th International Conference on Hybrid Systems, 163–72. ACM, 2017. https://doi.org/10.1145/3049797.3049814.","ieee":"H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, and T. A. Henzinger, “Safety verification of nonlinear hybrid systems based on invariant clusters,” in Proceedings of the 20th International Conference on Hybrid Systems, Pittsburgh, PA, United States, 2017, pp. 163–172.","short":"H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, T.A. Henzinger, in:, Proceedings of the 20th International Conference on Hybrid Systems, ACM, 2017, pp. 163–172.","ama":"Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. Safety verification of nonlinear hybrid systems based on invariant clusters. In: Proceedings of the 20th International Conference on Hybrid Systems. ACM; 2017:163-172. doi:10.1145/3049797.3049814","apa":"Kong, H., Bogomolov, S., Schilling, C., Jiang, Y., & Henzinger, T. A. (2017). Safety verification of nonlinear hybrid systems based on invariant clusters. In Proceedings of the 20th International Conference on Hybrid Systems (pp. 163–172). Pittsburgh, PA, United States: ACM. https://doi.org/10.1145/3049797.3049814","mla":"Kong, Hui, et al. “Safety Verification of Nonlinear Hybrid Systems Based on Invariant Clusters.” Proceedings of the 20th International Conference on Hybrid Systems, ACM, 2017, pp. 163–72, doi:10.1145/3049797.3049814."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"type":"journal_article","status":"public","_id":"667","article_number":"2786","author":[{"id":"3E57A680-F248-11E8-B48F-1D18A9856A87","first_name":"Gaia","last_name":"Novarino","orcid":"0000-0002-7673-7178","full_name":"Novarino, Gaia"}],"publist_id":"7060","title":"The antisocial side of antibiotics","department":[{"_id":"GaNo"}],"citation":{"ieee":"G. Novarino, “The antisocial side of antibiotics,” Science Translational Medicine, vol. 9, no. 387. American Association for the Advancement of Science, 2017.","short":"G. Novarino, Science Translational Medicine 9 (2017).","ama":"Novarino G. The antisocial side of antibiotics. Science Translational Medicine. 2017;9(387). doi:10.1126/scitranslmed.aan2786","apa":"Novarino, G. (2017). The antisocial side of antibiotics. Science Translational Medicine. American Association for the Advancement of Science. https://doi.org/10.1126/scitranslmed.aan2786","mla":"Novarino, Gaia. “The Antisocial Side of Antibiotics.” Science Translational Medicine, vol. 9, no. 387, 2786, American Association for the Advancement of Science, 2017, doi:10.1126/scitranslmed.aan2786.","ista":"Novarino G. 2017. The antisocial side of antibiotics. Science Translational Medicine. 9(387), 2786.","chicago":"Novarino, Gaia. “The Antisocial Side of Antibiotics.” Science Translational Medicine. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/scitranslmed.aan2786."},"date_updated":"2021-01-12T08:08:30Z","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","scopus_import":1,"publisher":"American Association for the Advancement of Science","intvolume":" 9","month":"04","abstract":[{"text":"Perinatal exposure to penicillin may result in longlasting gut and behavioral changes.","lang":"eng"}],"oa_version":"None","date_created":"2018-12-11T11:47:48Z","doi":"10.1126/scitranslmed.aan2786","issue":"387","date_published":"2017-04-26T00:00:00Z","volume":9,"publication_status":"published","year":"2017","publication_identifier":{"issn":["19466234"]},"language":[{"iso":"eng"}],"publication":"Science Translational Medicine","day":"26"},{"department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:37Z","date_updated":"2021-01-12T08:08:34Z","ddc":["570"],"type":"journal_article","article_type":"original","status":"public","_id":"668","volume":292,"issue":"17","publication_identifier":{"issn":["00219258"]},"publication_status":"published","file":[{"file_name":"2017_JBC_Horsthemke.pdf","date_created":"2019-10-24T15:25:42Z","file_size":5647880,"date_updated":"2020-07-14T12:47:37Z","creator":"dernst","file_id":"6971","checksum":"d488162874326a4bb056065fa549dc4a","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"language":[{"iso":"eng"}],"scopus_import":1,"month":"04","intvolume":" 292","abstract":[{"lang":"eng","text":"Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading."}],"oa_version":"Published Version","publist_id":"7059","author":[{"first_name":"Markus","last_name":"Horsthemke","full_name":"Horsthemke, Markus"},{"first_name":"Anne","full_name":"Bachg, Anne","last_name":"Bachg"},{"last_name":"Groll","full_name":"Groll, Katharina","first_name":"Katharina"},{"full_name":"Moyzio, Sven","last_name":"Moyzio","first_name":"Sven"},{"last_name":"Müther","full_name":"Müther, Barbara","first_name":"Barbara"},{"full_name":"Hemkemeyer, Sandra","last_name":"Hemkemeyer","first_name":"Sandra"},{"first_name":"Roland","last_name":"Wedlich Söldner","full_name":"Wedlich Söldner, Roland"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"first_name":"Sebastian","full_name":"Tacke, Sebastian","last_name":"Tacke"},{"first_name":"Martin","full_name":"Bähler, Martin","last_name":"Bähler"},{"last_name":"Hanley","full_name":"Hanley, Peter","first_name":"Peter"}],"title":"Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion","citation":{"ista":"Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273.","chicago":"Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923.","short":"M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273.","ieee":"M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017.","ama":"Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923","apa":"Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923","mla":"Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","page":"7258 - 7273","doi":"10.1074/jbc.M116.766923","date_published":"2017-04-28T00:00:00Z","date_created":"2018-12-11T11:47:49Z","has_accepted_license":"1","year":"2017","day":"28","publication":"Journal of Biological Chemistry","quality_controlled":"1","publisher":"American Society for Biochemistry and Molecular Biology","oa":1},{"type":"journal_article","article_type":"original","status":"public","_id":"669","department":[{"_id":"JiFr"}],"file_date_updated":"2020-07-14T12:47:37Z","date_updated":"2021-01-12T08:08:35Z","ddc":["580"],"scopus_import":1,"intvolume":" 174","month":"05","abstract":[{"lang":"eng","text":"The exocyst, a eukaryotic tethering complex, coregulates targeted exocytosis as an effector of small GTPases in polarized cell growth. In land plants, several exocyst subunits are encoded by double or triple paralogs, culminating in tens of EXO70 paralogs. Out of 23 Arabidopsis thaliana EXO70 isoforms, we analyzed seven isoforms expressed in pollen. Genetic and microscopic analyses of single mutants in EXO70A2, EXO70C1, EXO70C2, EXO70F1, EXO70H3, EXO70H5, and EXO70H6 genes revealed that only a loss-of-function EXO70C2 allele resulted in a significant male-specific transmission defect (segregation 40%:51%:9%) due to aberrant pollen tube growth. Mutant pollen tubes grown in vitro exhibited an enhanced growth rate and a decreased thickness of the tip cell wall, causing tip bursts. However, exo70C2 pollen tubes could frequently recover and restart their speedy elongation, resulting in a repetitive stop-and-go growth dynamics. A pollenspecific depletion of the closest paralog, EXO70C1, using artificial microRNA in the exo70C2 mutant background, resulted in a complete pollen-specific transmission defect, suggesting redundant functions of EXO70C1 and EXO70C2. Both EXO70C1 and EXO70C2, GFP tagged and expressed under the control of their native promoters, localized in the cytoplasm of pollen grains, pollen tubes, and also root trichoblast cells. The expression of EXO70C2-GFP complemented the aberrant growth of exo70C2 pollen tubes. The absent EXO70C2 interactions with core exocyst subunits in the yeast two-hybrid assay, cytoplasmic localization, and genetic effect suggest an unconventional EXO70 function possibly as a regulator of exocytosis outside the exocyst complex. In conclusion, EXO70C2 is a novel factor contributing to the regulation of optimal tip growth of Arabidopsis pollen tubes. "}],"oa_version":"Submitted Version","pmid":1,"issue":"1","volume":174,"publication_status":"published","publication_identifier":{"issn":["00320889"]},"language":[{"iso":"eng"}],"file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"7041","checksum":"97155acc6aa5f0d0a78e0589a932fe02","creator":"dernst","date_updated":"2020-07-14T12:47:37Z","file_size":2176903,"date_created":"2019-11-18T16:16:18Z","file_name":"2017_PlantPhysio_Synek.pdf"}],"external_id":{"pmid":["28356503"]},"article_processing_charge":"No","publist_id":"7058","author":[{"full_name":"Synek, Lukáš","last_name":"Synek","first_name":"Lukáš"},{"first_name":"Nemanja","last_name":"Vukašinović","full_name":"Vukašinović, Nemanja"},{"first_name":"Ivan","full_name":"Kulich, Ivan","last_name":"Kulich"},{"last_name":"Hála","full_name":"Hála, Michal","first_name":"Michal"},{"first_name":"Klára","full_name":"Aldorfová, Klára","last_name":"Aldorfová"},{"first_name":"Matyas","id":"43905548-F248-11E8-B48F-1D18A9856A87","full_name":"Fendrych, Matyas","orcid":"0000-0002-9767-8699","last_name":"Fendrych"},{"first_name":"Viktor","last_name":"Žárský","full_name":"Žárský, Viktor"}],"title":"EXO70C2 is a key regulatory factor for optimal tip growth of pollen","citation":{"chicago":"Synek, Lukáš, Nemanja Vukašinović, Ivan Kulich, Michal Hála, Klára Aldorfová, Matyas Fendrych, and Viktor Žárský. “EXO70C2 Is a Key Regulatory Factor for Optimal Tip Growth of Pollen.” Plant Physiology. American Society of Plant Biologists, 2017. https://doi.org/10.1104/pp.16.01282.","ista":"Synek L, Vukašinović N, Kulich I, Hála M, Aldorfová K, Fendrych M, Žárský V. 2017. EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. 174(1), 223–240.","mla":"Synek, Lukáš, et al. “EXO70C2 Is a Key Regulatory Factor for Optimal Tip Growth of Pollen.” Plant Physiology, vol. 174, no. 1, American Society of Plant Biologists, 2017, pp. 223–40, doi:10.1104/pp.16.01282.","apa":"Synek, L., Vukašinović, N., Kulich, I., Hála, M., Aldorfová, K., Fendrych, M., & Žárský, V. (2017). EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. American Society of Plant Biologists. https://doi.org/10.1104/pp.16.01282","ama":"Synek L, Vukašinović N, Kulich I, et al. EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. 2017;174(1):223-240. doi:10.1104/pp.16.01282","short":"L. Synek, N. Vukašinović, I. Kulich, M. Hála, K. Aldorfová, M. Fendrych, V. Žárský, Plant Physiology 174 (2017) 223–240.","ieee":"L. Synek et al., “EXO70C2 is a key regulatory factor for optimal tip growth of pollen,” Plant Physiology, vol. 174, no. 1. American Society of Plant Biologists, pp. 223–240, 2017."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"quality_controlled":"1","publisher":"American Society of Plant Biologists","page":"223 - 240","date_created":"2018-12-11T11:47:49Z","date_published":"2017-05-01T00:00:00Z","doi":"10.1104/pp.16.01282","year":"2017","has_accepted_license":"1","publication":"Plant Physiology","day":"01"},{"type":"journal_article","status":"public","_id":"671","department":[{"_id":"KrCh"}],"date_updated":"2021-01-12T08:08:37Z","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5422766/","open_access":"1"}],"scopus_import":1,"intvolume":" 114","month":"05","abstract":[{"text":"Humans routinely use conditionally cooperative strategies when interacting in repeated social dilemmas. They are more likely to cooperate if others cooperated before, and are ready to retaliate if others defected. To capture the emergence of reciprocity, most previous models consider subjects who can only choose from a restricted set of representative strategies, or who react to the outcome of the very last round only. As players memorize more rounds, the dimension of the strategy space increases exponentially. This increasing computational complexity renders simulations for individuals with higher cognitive abilities infeasible, especially if multiplayer interactions are taken into account. Here, we take an axiomatic approach instead. We propose several properties that a robust cooperative strategy for a repeated multiplayer dilemma should have. These properties naturally lead to a unique class of cooperative strategies, which contains the classical Win-Stay Lose-Shift rule as a special case. A comprehensive numerical analysis for the prisoner's dilemma and for the public goods game suggests that strategies of this class readily evolve across various memory-n spaces. Our results reveal that successful strategies depend not only on how cooperative others were in the past but also on the respective context of cooperation.","lang":"eng"}],"oa_version":"Published Version","pmid":1,"ec_funded":1,"volume":114,"issue":"18","publication_status":"published","publication_identifier":{"issn":["00278424"]},"language":[{"iso":"eng"}],"project":[{"name":"Quantitative Graph Games: Theory and Applications","grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"grant_number":"P 23499-N23","name":"Modern Graph Algorithmic Techniques in Formal Verification","_id":"2584A770-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FWF","_id":"25863FF4-B435-11E9-9278-68D0E5697425","name":"Game Theory","grant_number":"S11407"}],"external_id":{"pmid":["28420786"]},"article_processing_charge":"Yes (in subscription journal)","author":[{"last_name":"Hilbe","orcid":"0000-0001-5116-955X","full_name":"Hilbe, Christian","id":"2FDF8F3C-F248-11E8-B48F-1D18A9856A87","first_name":"Christian"},{"last_name":"Martinez","full_name":"Martinez, Vaquero","first_name":"Vaquero"},{"last_name":"Chatterjee","full_name":"Chatterjee, Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","first_name":"Krishnendu"},{"first_name":"Martin","full_name":"Nowak, Martin","last_name":"Nowak"}],"publist_id":"7053","title":"Memory-n strategies of direct reciprocity","citation":{"ama":"Hilbe C, Martinez V, Chatterjee K, Nowak M. Memory-n strategies of direct reciprocity. PNAS. 2017;114(18):4715-4720. doi:10.1073/pnas.1621239114","apa":"Hilbe, C., Martinez, V., Chatterjee, K., & Nowak, M. (2017). Memory-n strategies of direct reciprocity. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1621239114","ieee":"C. Hilbe, V. Martinez, K. Chatterjee, and M. Nowak, “Memory-n strategies of direct reciprocity,” PNAS, vol. 114, no. 18. National Academy of Sciences, pp. 4715–4720, 2017.","short":"C. Hilbe, V. Martinez, K. Chatterjee, M. Nowak, PNAS 114 (2017) 4715–4720.","mla":"Hilbe, Christian, et al. “Memory-n Strategies of Direct Reciprocity.” PNAS, vol. 114, no. 18, National Academy of Sciences, 2017, pp. 4715–20, doi:10.1073/pnas.1621239114.","ista":"Hilbe C, Martinez V, Chatterjee K, Nowak M. 2017. Memory-n strategies of direct reciprocity. PNAS. 114(18), 4715–4720.","chicago":"Hilbe, Christian, Vaquero Martinez, Krishnendu Chatterjee, and Martin Nowak. “Memory-n Strategies of Direct Reciprocity.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1621239114."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa":1,"quality_controlled":"1","publisher":"National Academy of Sciences","page":"4715 - 4720","date_created":"2018-12-11T11:47:50Z","date_published":"2017-05-02T00:00:00Z","doi":"10.1073/pnas.1621239114","year":"2017","publication":"PNAS","day":"02"},{"day":"01","publication":"Computer Graphics Forum","year":"2017","date_published":"2017-05-01T00:00:00Z","doi":"10.1111/cgf.13110","date_created":"2018-12-11T11:47:49Z","page":"95 - 106","publisher":"Wiley","quality_controlled":"1","oa":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Schreck, Camille, et al. “Interactive Paper Tearing.” Computer Graphics Forum, vol. 36, no. 2, Wiley, 2017, pp. 95–106, doi:10.1111/cgf.13110.","apa":"Schreck, C., Rohmer, D., & Hahmann, S. (2017). Interactive paper tearing. Computer Graphics Forum. Wiley. https://doi.org/10.1111/cgf.13110","ama":"Schreck C, Rohmer D, Hahmann S. Interactive paper tearing. Computer Graphics Forum. 2017;36(2):95-106. doi:10.1111/cgf.13110","short":"C. Schreck, D. Rohmer, S. Hahmann, Computer Graphics Forum 36 (2017) 95–106.","ieee":"C. Schreck, D. Rohmer, and S. Hahmann, “Interactive paper tearing,” Computer Graphics Forum, vol. 36, no. 2. Wiley, pp. 95–106, 2017.","chicago":"Schreck, Camille, Damien Rohmer, and Stefanie Hahmann. “Interactive Paper Tearing.” Computer Graphics Forum. Wiley, 2017. https://doi.org/10.1111/cgf.13110.","ista":"Schreck C, Rohmer D, Hahmann S. 2017. Interactive paper tearing. Computer Graphics Forum. 36(2), 95–106."},"title":"Interactive paper tearing","author":[{"id":"2B14B676-F248-11E8-B48F-1D18A9856A87","first_name":"Camille","last_name":"Schreck","full_name":"Schreck, Camille"},{"full_name":"Rohmer, Damien","last_name":"Rohmer","first_name":"Damien"},{"first_name":"Stefanie","full_name":"Hahmann, Stefanie","last_name":"Hahmann"}],"publist_id":"7056","article_processing_charge":"No","project":[{"_id":"25357BD2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Deep Pictures: Creating Visual and Haptic Vector Images","grant_number":"P 24352-N23"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["01677055"]},"publication_status":"published","volume":36,"issue":"2","oa_version":"Published Version","abstract":[{"text":"We propose an efficient method to model paper tearing in the context of interactive modeling. The method uses geometrical information to automatically detect potential starting points of tears. We further introduce a new hybrid geometrical and physical-based method to compute the trajectory of tears while procedurally synthesizing high resolution details of the tearing path using a texture based approach. The results obtained are compared with real paper and with previous studies on the expected geometric paths of paper that tears.","lang":"eng"}],"month":"05","intvolume":" 36","scopus_import":1,"main_file_link":[{"url":"https://hal.inria.fr/hal-01647113/file/eg_2017_schreck_paper_tearing.pdf","open_access":"1"}],"ddc":["000"],"date_updated":"2021-01-12T08:08:37Z","department":[{"_id":"ChWo"}],"_id":"670","status":"public","type":"journal_article","article_type":"original"},{"publication_identifier":{"issn":["22111247"]},"publication_status":"published","file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"5109","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","creator":"system","date_updated":"2020-07-14T12:47:38Z","file_size":2248814,"date_created":"2018-12-12T10:14:54Z","file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf"}],"language":[{"iso":"eng"}],"volume":19,"issue":"5","ec_funded":1,"abstract":[{"lang":"eng","text":"Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration."}],"oa_version":"Published Version","scopus_import":1,"month":"05","intvolume":" 19","date_updated":"2023-02-23T12:50:09Z","ddc":["570"],"department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"file_date_updated":"2020-07-14T12:47:38Z","_id":"672","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"status":"public","pubrep_id":"900","has_accepted_license":"1","year":"2017","day":"02","publication":"Cell Reports","page":"902 - 909","date_published":"2017-05-02T00:00:00Z","doi":"10.1016/j.celrep.2017.04.027","date_created":"2018-12-11T11:47:50Z","publisher":"Cell Press","quality_controlled":"1","oa":1,"citation":{"chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.","ista":"Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.","mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.","ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","ieee":"K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"7052","author":[{"orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","last_name":"Vaahtomeri","first_name":"Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","full_name":"Brown, Markus","last_name":"Brown"},{"first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","last_name":"Hauschild"},{"first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"last_name":"Leithner","full_name":"Leithner, Alexander F","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Mehling","full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","first_name":"Matthias","id":"3C23B994-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kaufmann","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","first_name":"Walter"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"article_processing_charge":"Yes","title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","project":[{"grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}]},{"scopus_import":1,"intvolume":" 27","month":"05","abstract":[{"text":"Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo.","lang":"eng"}],"oa_version":"None","ec_funded":1,"volume":27,"issue":"9","publication_status":"published","publication_identifier":{"issn":["09609822"]},"language":[{"iso":"eng"}],"type":"journal_article","status":"public","_id":"674","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"date_updated":"2023-02-23T12:50:44Z","publisher":"Cell Press","quality_controlled":"1","page":"1314 - 1325","date_created":"2018-12-11T11:47:51Z","doi":"10.1016/j.cub.2017.04.004","date_published":"2017-05-09T00:00:00Z","year":"2017","publication":"Current Biology","day":"09","project":[{"call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme","grant_number":"291734"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}],"author":[{"first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","full_name":"Schwarz, Jan"},{"full_name":"Bierbaum, Veronika","last_name":"Bierbaum","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","first_name":"Veronika"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari","orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","last_name":"Vaahtomeri"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"last_name":"Brown","full_name":"Brown, Markus","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"De Vries, Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","last_name":"Leithner"},{"full_name":"Reversat, Anne","orcid":"0000-0003-0666-8928","last_name":"Reversat","id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne"},{"last_name":"Merrin","full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","id":"4515C308-F248-11E8-B48F-1D18A9856A87","first_name":"Jack"},{"last_name":"Tarrant","full_name":"Tarrant, Teresa","first_name":"Teresa"},{"id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Tobias","full_name":"Bollenbach, Tobias","orcid":"0000-0003-4398-476X","last_name":"Bollenbach"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"7050","title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","citation":{"ista":"Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.","chicago":"Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.","apa":"Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004","ama":"Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004","short":"J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325.","ieee":"J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.","mla":"Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004."},"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87"},{"date_updated":"2021-01-12T08:08:57Z","ddc":["570"],"file_date_updated":"2020-07-14T12:47:40Z","department":[{"_id":"MiSi"}],"_id":"677","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"status":"public","pubrep_id":"899","publication_identifier":{"issn":["22111247"]},"publication_status":"published","file":[{"date_created":"2018-12-12T10:15:48Z","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","date_updated":"2020-07-14T12:47:40Z","file_size":3005610,"creator":"system","checksum":"efc7287d9c6354983cb151880e9ad72a","file_id":"5171","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"language":[{"iso":"eng"}],"issue":"7","volume":19,"abstract":[{"lang":"eng","text":"The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR."}],"oa_version":"Published Version","scopus_import":1,"month":"05","intvolume":" 19","citation":{"apa":"Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051","ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051","ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.","ista":"Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303.","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Lademann","full_name":"Lademann, Claudio","first_name":"Claudio"},{"last_name":"Renkawitz","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369","first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Pfander","full_name":"Pfander, Boris","first_name":"Boris"},{"full_name":"Jentsch, Stefan","last_name":"Jentsch","first_name":"Stefan"}],"publist_id":"7046","title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","has_accepted_license":"1","year":"2017","day":"16","publication":"Cell Reports","page":"1294 - 1303","doi":"10.1016/j.celrep.2017.04.051","date_published":"2017-05-16T00:00:00Z","date_created":"2018-12-11T11:47:52Z","quality_controlled":"1","publisher":"Cell Press","oa":1}]